KNOCKOUT OF CALCIUM-INDEPENDENT PHOSPHOLIPASE A2BETA ATTENUATES ENDOTHELIUM

敲除钙依赖性磷脂酶 A2β 会削弱内皮细胞

• 批准号: 7954029
• 负责人: HANS H DIETRICH
• 金额: $ 0.76万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-02-01 至 2010-01-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7954029
• 关键词: Acetylcholine; Arachidonic Acids; Attenuated; Blood Vessels; Calcium; Caliber; Computer Retrieval of Information on Scientific Projects Database; Endothelium; Funding; Grant; Institution; Knock-out; Lysophospholipids; Mass Spectrum Analysis; Measures; Mesentery; Mus; Phenylephrine; Phospholipase; Play; Protein Isoforms; Relaxation; Research; Research Personnel; Resources; Role; Source; United States National Institutes of Health; Vascular Smooth Muscle; Vasodilation; arteriole; base; biomedical resource; constriction; human PLA2G6 protein

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The mechanisms regulating constriction and relaxation of vascular smooth muscle in healthy and diseased blood vessels are incompletely understood, but the activation of one or more phospholipases leading to the initial release of arachidonic acid and lysophospholipids play prominent roles. To identify the role of specific phospholipases in the constriction of mesenteric arterioles induced by phenylephrine (PE) and endothelium-dependent vasodilation induced by acetylcholine (ACh), we measured changes in the diameter of second- and third-order mesenteric arterioles isolated from mice lacking the ¿ isoform of calcium-independent phospholipase A2 (iPLA2¿-/-) as well as inhibition of iPLA2b in wild-type vessels using mechanism based inhibition.

该副本是使用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这是调查员的机构。 在健康和解散的血管中调节血管平滑肌的机制和松弛尚不完全了解，但是一种或多种磷脂酶的激活导致蛛网膜酸和溶血磷脂的初始释放起着重要作用。为了确定特定磷脂酶在乙酰胆碱诱导的（PE）和内皮依赖性的乙酰胆碱（ACH）诱导的肠系膜artiolles的收缩中的作用，我们测量了从二阶和第三阶小动脉中的直径的变化，这些小动脉均未依赖于隔离的小鼠的含量ph，均属于渗透的小鼠的含量层ph （IPLA2¿-/ - ）以及使用基于机制的抑制作用在野生型vissels中对IPLA2B的抑制。